EP-A-0 565 909 (issued to Sorin Biomedica Cardio SpA) describes a device in which the sympathico-vagal activity is analyzed based upon the cardiac signal collected (sensed) by endocavitary electrodes, in particular by an analysis of the variability of RR intervals (intervals separating two consecutive spontaneous ventricular depolarizations). Interest in monitoring the sympathico-vagal activity arises from the possibility of predicting the imminent occurrence of a syncope of vaso-vagal origin, and preventing its occurrence by an adapted therapy, typically (but not exclusively) an antibradycardiac stimulation therapy.
Primarily, a syncope is a temporary loss of consciousness with a fall in the muscular tone, resulting from the temporary reduction of cerebral circulation. Among various types of syncopes, the vaso-vagal syncope is caused by a temporary imbalance of the regulation system of the vaso-vagal balance. This leads to an excessive activation of the vagal system, in turn resulting in a vasodilatation and a bradycardia leading to the syncope. One can anticipate syncope by a certain number of precursory signs. It is desirable among patients carrying a cardiac pacemaker to detect a risk of imminent occurrence of such a syncope and to apply a suitable therapy and to avoid the fainting of the patient.
It is generally considered that the vaso-vagal syncope comes from a state where the sympathetic nerve system has a particularly high reactivity that initiates an antagonistic response of the parasympathetic system, causing in turn a vasodilatation inducing a reduction of the filling of the ventricles and the bradycardia. Because the chain of events leading to the syncope begins several minutes before the loss of consciousness occurs, it is desirable to be able to detect such a state as soon as possible to be able to take the suitable required measures.
It is, however, unfortunately not possible to directly measure the balance of the autonomous nervous system. It is only possible to evaluate this state in an indirect manner based upon various physiological parameters such as the heartbeat rate, the myocardic contractility, the ventilatory activity or other parameters, or a combination of these various parameters. The known techniques, however, appear difficult to implement, taking into account in particular the multiplicity of the factors likely to modify the heartbeat rate, factors which are not necessarily related to an imbalance of the sympathico-vagal system.
The present invention has as an objective proposing an alternative approach to the analysis of the sympathico-vagal activity by an implanted device, while proposing to implement a detection based on the analysis of endocardiac acceleration, more particularly an analysis of the peaks of endocardiac acceleration.
One can collect (i.e., detect or sense) an endocardiac acceleration signal, as described in EP-A-0 515 319 (assigned to Sorin Biomedica Cardio SpA), which describes a endocavitary probe equipped with a distal stimulation electrode located at the bottom of the ventricle, and a micro-accelerometer able to measure the endocardiac acceleration. The endocardiac acceleration signal thus measured during a cardiac cycle forms, inter alia, two peaks corresponding to the two major noises that it is possible to recognize in each cycle of a healthy heart.
EP-A-0 655 260 (Sorin Biomedica Cardio SpA) describes a manner of processing the endocavitary acceleration signal delivered by the sensor located in the extremity of a probe to derive from it, in particular, the two peak values of endocardiac acceleration, useful in particular for the detection of cardiac disorders and the release (or not) of a therapy, for example, an antibradycardiac stimulation therapy accelerating the stimulation rate. The first peak of endocardiac acceleration (“PEA I”) corresponds to the closing of the mitral and tricuspid valves, at the beginning of the isovolumic phase of ventricular contraction (i.e., the systole). The variations of this first peak are closely related to the variations of the pressure in the ventricle (the amplitude of peak PEA I, more precisely, being correlated to the positive maximum of the pressure variation dP/dt in the left ventricle) and can thus constitute a parameter representative of the contractility of the myocardium, itself related to the level of activity of the sympathetic nerve system. The second peak of endocardiac acceleration (“PEA II”) corresponds to the closing of the aortic and pulmonary valves, at the moment of the isovolumic ventricular relaxation phase. This second peak, which is produced by the abrupt deceleration of the blood mass moving in the aorta, constitutes a parameter representative of the peripheral blood pressure at the beginning of the diastole.
The invention proposes to use this information for heretofore unknown and different purposes, namely, to analyze the sympathico-vagal activity of the patient.